First of all, I want to try to explain why we try to do that trial, which was at the beginning a little bit hard to get patients in. But we know from science that ACPAs emerge years before the onset of overt rheumatoid arthritis. So we could measure antibodies in the blood of healthy individuals, perhaps. This is due to genetics and environment.
And this is the asymptomatic phase in the development of RA. Later on we do have the symptomatic phase, which means that the patient is complaining about arthralgia and we can see by imaging techniques, like ultrasound or MRI, we could detect subclinical inflammation in these patients.
Going on with that, the patients present later the clinical overt arthritis, which means that the patient do have swollen joints, tender joints. We do have an elevated DAS28, perhaps. And if that will be not treated, the patients will have structural damage in the joints. So from that point of view, we normally try to keep the patient-- or we try to treat the patient as early as possible, which means actually in the first six months. But this is when the rheumatoid arthritis can be diagnosed by classification and diagnosis criteria.
What we try with our study is to treat the patient as early as possible. That means for us in the symptomatic phase where the patient is complaining about arthralgia for more than six weeks and where we can detect by MRI subclinical inflammation. This is our windows of opportunity, perhaps, to prevent or delay the onset of rheumatoid arthritis.
The main findings for this presentation is the treatment phase for the first six months. So we randomized the patients into placebo group and treatment group, which means that the patients in the treatment group did get abatacept for six months and then we have a follow-up phase for 12 months. What we have seen is the findings-- what we could detect is that-- and this was the primary endpoint of our study-- that the patient must have an improvement in MRI signs of synovitis, tenosynovitis, or osteitis between baseline and six months.
And what we have seen is that more than 60% in the abatacept group did have this improvement, while the other group of the placebo-treated patients-- only 30% of the patients could show that. So this was statistically highly significant. And so with that, this wasn't a successful trial.
But further on, we also measured if patients may have an early termination in each group. And there we also have seen that only seven patients in the abatacept group did have an early termination while in the placebo group 21%-- 21 patients, which means 33% of the patients, did have an early termination. And this was also highly significant.
So we also saw that in the treatment group with abatacept, only four patients did have a progression to arthritis and with that the diagnosis of rheumatoid arthritis, while 17 patients, which means 35% of the patients, did have that in the placebo group.
So they develop rheumatoid arthritis then. So this is our findings for now and we're looking forward for the results of the 18 months, which means after six months of treatment, 12 months of follow-up with no treatment. We will see how these patients present then. We know from the clinical side that there are still significant difference between abatacept-treated patients than placebo-treated patients.
First of all, it is that-- if the use of abatacept in RA at-risk patients, this is a safe treatment with no new safety issues coming up in this trial. With abatacept, we have a superior situation versus placebo in improving subclinical inflammation in RA at-risk patients and we are inhibiting the progression to arthritis in the first six months, but also in the 12 months of follow-up.
So we should discuss for the future, if we will not better treat patients with clinical symptoms, like arthralgia and showing up with inflammation-- subclinical inflammation by imaging techniques-- if we should not treat them with such drugs to prevent or even delay the onset of RA.
At the moment, there was the PRAIRI trial, which happened a while ago, where the patients were treated with rituximab and they could also show a delay of the onset of RA and even abatacept did that. We do not-- or we know that other drugs like IL-6 receptor inhibitors or TNF blockers will not do that because they will not decrease the antibody levels of ACPA which seem to be important for that, just adding the JAK inhibitors because they have also not shown that, for now-- that the JAK inhibitors may have a decrease in antibody levels or could show that. So it might be the same situation.